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Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg)

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE181133 | GEO | 2021/07/30

REPOSITORIES: GEO

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Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg) II

Project description:Purpose: Next-generation sequencing (NGS) has used to detect alterations in cellular pathways by various drugs. The goal of this study is to identify alteration of gene expression in human osteochondromas in response to identify nontreated or RARg agonist-treated osteochondorma transcriptome profiling (RNA-seq) and to evaluate the actions of RARg agonists on osteochondromas. Methods: Osteochondroma mRNA profiles of untreated or RARg agonist treated (4 days) osteochondroma explants were generated by deep sequencing, in triplicate, using Illumina HiSeq 4000. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results and Conclusions: Our study represents the detailed analysis of human osteochondromas, with biologic replicates, generated by RNA-seq technology. We conclude that RNA-seq based transcriptome revealed that RARg agonists acts on human osteochondromas and altered various types of biological functions.

2021-07-30 | GSE181129 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg) I

2021-07-26 | GSE180764 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg)

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg)

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Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg) I

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Gene expression profiles of MCF7 with with the following NR ligands: estradiol/E2 (ERÎ± agonist), AM580 (RARA agonist), CD437 (RARG agonist), ATRA (RARA/RARG agonist), GW0742 (PPARD agonist), R5020 (PGR agonist), and dexamethasone (GR/NR3C1 agonist).

Project description:Altered gene expression patterns in human diseases reflect perturbations in the transcriptional networks that regulate cellular state. In breast cancer, Nuclear Receptors (NRs) play a prominent role in governing gene expression. NRs have prognostic utility and are therapeutically important targets. In order to understand the function of nuclear receptors in breast cancer, we treated MCF7 cells with 6 nuclear receptor agonist, and performed expression arrrays with three biological replicates each. MCF-7 cells were cultured for 48 hours in medium with 10% charcoal-stripped FBS, and then were treated with 6 diffferent NR ligand (E2, AM580, CD437, ATRA, R5020, DEX) separately for 24h before collection and processing for microarrays. Three biological replicates were collected and processed for both control and treatment. with the 100nM GW0742 (PPARD specific ligand) and 100nM ATRA (RARs ligand), then collected after 24h for microarray processing. Controls were non-treated MCF7 cells. Both treatments and controls have three biological replicates.

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Gene expression profiles of MCF7 with with the following NR ligands: estradiol/E2 (ER? agonist), AM580 (RARA agonist), CD437 (RARG agonist), ATRA (RARA/RARG agonist), GW0742 (PPARD agonist), R5020 (PGR agonist), and dexamethasone (GR/NR3C1 agonist)

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Retinoic acid receptor γ (Rarg) and nuclear receptor subfamily 5, group A, member 2 (Nr5a2) promote conversion of fibroblasts to functional neurons.

Project description:Somatic cells can be reprogrammed to neurons and various other cell types with retrovirus or lentivirus. The limitation of this technology is that these genome-integration viruses may increase the risk of gene mutation and cause insertional mutagenesis. We recently found that non-integration adenovirus carrying neuronal transcription factors can induce fibroblasts to neurons. However, the conversion efficiency by the adenovirus is lower than that of the retrovirus or lentivirus. Therefore, it is crucial to identify other factors or chemical compounds to obtain neurons with high efficiency. In this study we show that the combination of Rarg (retinoic acid receptor γ) and Nr5a2 (nuclear receptor subfamily 5, group A, member 2; also known as Lrh-1 (liver receptor homologue 1)) rapidly promote the iN cell maturation within 1 week and greatly facilitate the conversion with neuronal purities of ∼50% and yields of >130%. They also improve neuronal pattern formation, electrophysiological characteristics, and functional integration in vivo. Moreover, the chemical compound agonists to Rarg and Nr5a2 function effectively as well. This approach may be used for the generation and application of iN cells in regenerative medicine.

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Gene expression profiles of MCF7 with with the following NR ligands: estradiol/E2 (ERα agonist), AM580 (RARA agonist), CD437 (RARG agonist), ATRA (RARA/RARG agonist), GW0742 (PPARD agonist), R5020 (PGR agonist), and dexamethasone (GR/NR3C1 agonist).

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Project description:Estrogen Related Receptors (ERRs) are key regulators of energy homeostasis and play important role in the etiology of metabolic disorders, skeletal muscle related disorders, and neurodegenerative diseases. Among the three ERR isoforms, ERRα emerged as a potential drug target for metabolic and neurodegenerative diseases. Although ERRβ/γ selective agonist chemical tools have been identified, there are no chemical tools that effectively target ERRα agonism. We successfully engineered high affinity ERRα agonism into a chemical scaffold that displays selective ERRβ/γ agonist activity (GSK4716), providing novel ERRα/β/γ pan agonists that can be used as tools to probe the physiological roles of these nuclear receptors. We identified the structural requirements to enhance selectivity toward ERRα. Molecular modeling shows that our novel modulators have favorable binding modes in the LBP of ERRα and can induce conformational changes where Phe328 that originally occupies the pocket is dislocated to accommodate the ligands in a rather small cavity. The best agonists up-regulated the expression of target genes PGC-1α and PGC-1β, which are necessary to achieve maximal mitochondrial biogenesis. Moreover, they increased the mRNA levels of PDK4, which play an important role in energy homeostasis.

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